Translocation of the brain-type glucose transporter largely accounts for insulin stimulation of glucose transport in BC3H-1 myocytes

Insulin-stimulated glucose transport was examined in BC3H-1 myocytes. Insulin treatment lead to a 2.7 +/- 0.3-fold increase in the rate of deoxyglucose transport and, under the same conditions, a 2.1 +/- 0.1-fold increase in the amount of the brain-type glucose transporter (GLUT 1) at the cell surfa...

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Veröffentlicht in:	Biochemical journal 1990-08, Vol.269 (3), p.597-601
Hauptverfasser:	Calderhead, D M, Kitagawa, K, Lienhard, G E, Gould, G W
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Brain Chemistry Cell Line Cell Membrane - ultrastructure glucose insulin Insulin - pharmacology Mice Monosaccharide Transport Proteins - pharmacokinetics Muscles - analysis Muscles - cytology Muscles - metabolism myocytes Stimulation, Chemical
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container_title	Biochemical journal
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creator	Calderhead, D M Kitagawa, K Lienhard, G E Gould, G W
description	Insulin-stimulated glucose transport was examined in BC3H-1 myocytes. Insulin treatment lead to a 2.7 +/- 0.3-fold increase in the rate of deoxyglucose transport and, under the same conditions, a 2.1 +/- 0.1-fold increase in the amount of the brain-type glucose transporter (GLUT 1) at the cell surface. It has been shown that some insulin-responsive tissues express a second, immunologically distinct, transporter, namely GLUT 4. We report here that BC3H-1 myocytes and C2 and G8 myotubes express only GLUT 1; in contrast, rat soleus muscle and heart express 3-4 times higher levels of GLUT 4 than GLUT 1. Thus translocation of GLUT 1 can account for most, if not all, of the insulin stimulation of glucose transport in BC3H-1 myocytes. On the other, hand, neither BC3H-1 myocytes nor the other muscle-cell lines are adequate as models for the study of insulin regulation of glucose transport in muscle tissue.
doi_str_mv	10.1042/bj2690597
format	Article
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Insulin treatment lead to a 2.7 +/- 0.3-fold increase in the rate of deoxyglucose transport and, under the same conditions, a 2.1 +/- 0.1-fold increase in the amount of the brain-type glucose transporter (GLUT 1) at the cell surface. It has been shown that some insulin-responsive tissues express a second, immunologically distinct, transporter, namely GLUT 4. We report here that BC3H-1 myocytes and C2 and G8 myotubes express only GLUT 1; in contrast, rat soleus muscle and heart express 3-4 times higher levels of GLUT 4 than GLUT 1. Thus translocation of GLUT 1 can account for most, if not all, of the insulin stimulation of glucose transport in BC3H-1 myocytes. On the other, hand, neither BC3H-1 myocytes nor the other muscle-cell lines are adequate as models for the study of insulin regulation of glucose transport in muscle tissue.</description><subject>Animals</subject><subject>Brain Chemistry</subject><subject>Cell Line</subject><subject>Cell Membrane - ultrastructure</subject><subject>glucose</subject><subject>insulin</subject><subject>Insulin - pharmacology</subject><subject>Mice</subject><subject>Monosaccharide Transport Proteins - pharmacokinetics</subject><subject>Muscles - analysis</subject><subject>Muscles - cytology</subject><subject>Muscles - metabolism</subject><subject>myocytes</subject><subject>Stimulation, Chemical</subject><issn>0264-6021</issn><issn>1470-8728</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2LFDEURYMoYzu68AcIWQkuSl9epT6yEbRRRxhwM66LJPWqJ0MqaZOUUHt_uDVM0yguXL3FO_dw4TL2UsBbARLfmTtsFTSqe8R2QnZQ9R32j9kOsJVVCyiesmc53wEICRIu2AUiICq5Y79ukg7ZR6uLi4HHiZdb4iZpF6qyHokf_GJjJl7uuWNMhRL3Oh3Ir1xbG5dQMp9i4i7kxbvAc3Hz4s-6f_IbyD_u66tK8HmNdi2Un7Mnk_aZXpzuJfv--dPN_qq6_vbl6_7DdWUliFKNndBG1DRBj4SiF3Y0SmpARf0IUhuJsjdkalRNi6DBIJoeRpI4NpuivmTvH7zHxcw0WgpbKz8ck5t1Woeo3fD3J7jb4RB_DkLUosV-E7w-CVL8sVAuw-yyJe91oLjkoVOqxUbV_wVF00GrhNzANw-gTTHnRNO5jYDhftvhvO3Gvvqz_pk8jVn_BhjVonw</recordid><startdate>19900801</startdate><enddate>19900801</enddate><creator>Calderhead, D M</creator><creator>Kitagawa, K</creator><creator>Lienhard, G E</creator><creator>Gould, G W</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19900801</creationdate><title>Translocation of the brain-type glucose transporter largely accounts for insulin stimulation of glucose transport in BC3H-1 myocytes</title><author>Calderhead, D M ; Kitagawa, K ; Lienhard, G E ; Gould, G W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-d71ab13ef082e2181cdb94a029e8d04ab4248beb3295620a0b22b80de42d5c403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Animals</topic><topic>Brain Chemistry</topic><topic>Cell Line</topic><topic>Cell Membrane - ultrastructure</topic><topic>glucose</topic><topic>insulin</topic><topic>Insulin - pharmacology</topic><topic>Mice</topic><topic>Monosaccharide Transport Proteins - pharmacokinetics</topic><topic>Muscles - analysis</topic><topic>Muscles - cytology</topic><topic>Muscles - metabolism</topic><topic>myocytes</topic><topic>Stimulation, Chemical</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Calderhead, D M</creatorcontrib><creatorcontrib>Kitagawa, K</creatorcontrib><creatorcontrib>Lienhard, G E</creatorcontrib><creatorcontrib>Gould, G W</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biochemical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Calderhead, D M</au><au>Kitagawa, K</au><au>Lienhard, G E</au><au>Gould, G W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Translocation of the brain-type glucose transporter largely accounts for insulin stimulation of glucose transport in BC3H-1 myocytes</atitle><jtitle>Biochemical journal</jtitle><addtitle>Biochem J</addtitle><date>1990-08-01</date><risdate>1990</risdate><volume>269</volume><issue>3</issue><spage>597</spage><epage>601</epage><pages>597-601</pages><issn>0264-6021</issn><eissn>1470-8728</eissn><abstract>Insulin-stimulated glucose transport was examined in BC3H-1 myocytes. 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source	MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection
subjects	Animals Brain Chemistry Cell Line Cell Membrane - ultrastructure glucose insulin Insulin - pharmacology Mice Monosaccharide Transport Proteins - pharmacokinetics Muscles - analysis Muscles - cytology Muscles - metabolism myocytes Stimulation, Chemical
title	Translocation of the brain-type glucose transporter largely accounts for insulin stimulation of glucose transport in BC3H-1 myocytes
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